Deciphering the pathogenesis of tendinopathy: a three-stages process

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Abstract

Our understanding of the pathogenesis of “tendinopathy” is based on fragmented evidences like pieces of a jigsaw puzzle. We propose a “failed healing theory” to knit these fragments together, which can explain previous observations. We also propose that albeit “overuse injury” and other insidious “micro trauma” may well be primary triggers of the process, “tendinopathy” is not an “overuse injury” per se. The typical clinical, histological and biochemical presentation relates to a localized chronic pain condition which may lead to tendon rupture, the latter attributed to mechanical weakness. Characterization of pathological “tendinotic” tissues revealed coexistence of collagenolytic injuries and an active healing process, focal hypervascularity and tissue metaplasia. These observations suggest a failed healing process as response to a triggering injury. The pathogenesis of tendinopathy can be described as a three stage process: injury, failed healing and clinical presentation. It is likely that some of these “initial injuries” heal well and we speculate that predisposing intrinsic or extrinsic factors may be involved. The injury stage involves a progressive collagenolytic tendon injury. The failed healing stage mainly refers to prolonged activation and failed resolution of the normal healing process. Finally, the matrix disturbances, increased focal vascularity and abnormal cytokine profiles contribute to the clinical presentations of chronic tendon pain or rupture. With this integrative pathogenesis theory, we can relate the known manifestations of tendinopathy and point to the “missing links”. This model may guide future research on tendinopathy, until we could ultimately decipher the complete pathogenesis process and provide better treatments.

Introduction

In the past decades, our concepts on chronic tendon pain have evolved from “tendinitis” which focused on clinical inflammatory signs, into “tendinosis” which stressed the pathologic features of the free tendon as observed by histology and biochemistry, and then “tendinopathy” which declared nothing further about its nature, just introducing a new label for chronic tendon and insertion problems in general []. Woo and Renstrom [] concludes that the pathogenesis, etiology and mechanisms in most of the myriads of conditions related to tendinopathy are unknown. However, with clear definitions outlining and discriminating the various diagnoses of “tendinopathy”, it is still possible to propose a unified model for the pathogenesis based on available experimental evidences, which we propose as our theory to be proved or rejected by future investigation.

In general, tendinopathy is characterized by longstanding localized activity-related pain and the patients in general respond poorly to most “conservative treatments”. However, a wide spectrum of tendon pathologies is put under the umbrella entity of tendinopathy based on some common features [] (Table (Table1),1), leading to an impression that there is no single general pathogenesis or aetiology involved which can explain all conditions. If so, we firmly believe that these pathologies should be classified as different entities. As the current research evidences are confusing, it is very important to identify if there are common denominators and diversifiers for various manifestations of what we loosely call “tendinopathy” to help us understand the pathogeneses of these conditions.

Table 1

Involvement of failed healing in different manifestations of tendinopathies.

Injury Healing responses Failed Healing Histopathological changes Clinical presentation Different manifestations
• Overuse
• Previous traumatic injury
• Xenobiotics
• Pathogens
Inflammation Sustained pro-inflammatory cytokines • Pain
• Mechanical weakness
• “Tendinitis”
• Paratendinitis
• Insertional tendinopathy
• Overuse tendon injuries
• Spontaneous rupture
• Activity-related pain
• Calcified tendinopathy

Neovascularization Hypervascularity

Innervation Increased neuropeptides and innervation

Cell recruitment/apoptosis Hypercellularity, increased apoptosis

Matrix synthesis Mucoid, lipoid, calcific degeneration

Tenogenic differentiation/apoptosis

Matrix remodeling Collagenolysis, tendon adhesion

In this article, we review previous investigations according to the nature of the studies, for example, clinical observations, characterization of clinical samples, evaluation of treatments to patients with tendinopathy, animal models of tendinopathy and cell culture studies related to the effects of risk factors. Certainly we do not answer all questions with the integration of various research evidences, but we take the bold step to propose an integrative theory for the pathogenesis of tendinopathy based on the underlying messages in these studies.

Clinical observations of tendinopathy

To understand the pathogenesis of what today is labeled as “tendinopathy” we have to make some clear distinctions. Firstly we must consider the varying clinical presentations. Most tendon problems are presented to the clinician either as a rupture or localized pain, often including stiffness and swelling. Symptomatic tendinopathy refers to chronic localized pain with “degenerative” changes in tendons as observed by imaging or histology; while asymptomatic tendinopathy is identified from ruptures or partial rupture cases shown to be associated with non symptomatic pre-existing degenerative changes. Pathologies primarily manifested as passive loss of range of motion (i.e. trigger finger, frozen shoulder, etc) are not considered as tendinopathy in this discussion. Dating back to 1938, Codman reported degeneration in complete ruptures of rotator cuff []. Kannus and Josza reported in 1991 from a large number of histological samples that an absolute majority of patients with complete Achilles tendon ruptures had pathologic alterations which he described as “mucoid degeneration” []. This “mucoid degeneration” is almost equivalent to the histological alterations characterized for tendinosis []. It is very likely that these pathological changes in tendons imposed mechanical weakness and higher susceptibility to ruptures. Similar histopathological characteristics were also described in clinical samples of symptomatic tendinopathy [,]. It suggests that the “typical” histopathological changes characterized by tendon degeneration may not necessarily be directly linked to increased nociception giving the patients warning signals; while in painful cases, the mechanically weaker tendons may be protected from ruptures due to decreased impact levels since painful activities will be avoided.

Secondly, we must consider the etiology and epidemiology. Unfortunately, well defined epidemiological studies on “tendinopathy” are virtually nonexistent. Age-related changes in tendons were reported [], but tendinopathy is not an age-related degeneration because similar pathological changes are observed in young people []. Higher number of cases in males presented in clinical studies [,] may not reflect higher susceptibility of male gender to tendinopathy; on the contrary, it is reported that female gender was more susceptible to repetitive trauma in rotator cuff [] and female cyclists suffer a higher risk for “overuse injury” in general than their male counterparts []. There were significant gender differences in tendon microcirculation [] and the neuropeptide responsiveness in rabbit tendon explants was influenced by gender and pregnancy []. Diabetes [] and metabolic alterations such as dislipidemia [] has been proposed as risk factor for developing tendinopathy. These findings suggest that the hormonal background may affect the development of tendinopathy. Fluoroquinolone [] and corticosteroids [] were found to be associated with Achilles tendon ruptures; suggesting pharmacological influence on the development of tendon pathology. Overuse, repetitive strain or mechanical overload to tendons are considered as primary trigger of symptomatic tendinopathy in various regions [], as implied by the names such as “jumper’s knee”, “runner’s heel”, “swimmer’s shoulder” and “tennis elbow”. The prevalence of supraspinatous tendinopathy could be as high 69 % in elite swimmers []. However, there are frequent tendinopathy cases (pain or rupture) in the non-athlete population [,]. Thus overuse injury should not be equated to tendinopathy, but it may be one of the major triggers of the pathological development in some individuals. Furthermore, overuse as a risk factor for tendinopathy is not simply a quantitative increase in activities, but may also be attributed to improper gait or training errors [,].

Thirdly, the anatomical sites of tendinopathic changes add further complexity. Since overuse or cumulative trauma may also affect other peritendinous tissues, tendinopathy was sometimes presented with pathological changes in tenosynovium, bursa and nerves. Our discussion on the pathogenesis of tendinopathy should be focused on changes primarily initiated and observed in tendons; otherwise the pathogenesis pathways will be very heterogeneous. It follows that infectious tenosynovitis, bursitis, adhesive capsulitis or tendon and nerve entrapment in case of carpel tunnel syndrome will not be included in our model, but “paratenonitis” [] and “insertional tendinopathies” [] will be discussed since they are parts of a tendon. The pathological changes in different forms of tendinopathy are localized in different regions of the affected tendons, for example, the proximal deep posterior portion of the patellar tendon is affected in patellar tendinopathy, while mid-substance or insertion pathological changes can be observed in Achilles tendinopathy. The medial musculotendinous junction or lateral Humerus insertion was affected in Rotator cuff tendinopathy, while in lateral epicondylitis the fascial collagen structure on the extensor carpi radialis brevis tendon was pathological. Based on the involvement of pathological changes in the paratenon, different sub-classes can be further identified in Achilles tendinopathy []. Owing to these variations in the sites of pathological changes, it suggests the common denominator of the pathogenesis of tendinopathy may probably involve a process that can affect all parts of tendons [], including musculotendinous junction, mid-substance, insertion and paratenons. The “communication” between these structures around the tendons is poorly investigated.

Medical imaging of tendinopathy

Tendinopathy exhibited characteristic pathological changes which are visible under ultrasound or magnetic resonance imaging (MRI). Tendon thickening or swelling is revealed, localized hypoechogenic signals were detected by ultrasound [] and an increased T1 and T2 contrast signal was shown by MRI [,]. It suggests an increased water content which is probably related to increased accumulation of water-retaining proteoglycans. Doppler ultrasound imaging showed increased vascularity and blood flow in the pathological regions but the oxygen tension was not significantly different []. These findings suggested an inflammatory component [] with localized changes in the tendinous matrix and hypervascularity may be associated with the pathogenesis of tendinopathy.

Characterization of clinical samples of tendinopathy

Direct investigation of tendinopathy started with histological examination of the pathological tissues. Classical characteristics of “tendinosis” include degenerative changes in the collagenous matrix, hypercellularity, hypervascularity and a lack of inflammatory cells which has challenged the original misnomer “tendinitis” [,]. Further characterizations are basically extrapolation of these findings, for examples, measurement of proliferation and apoptosis to explain the changes in cellularity [,], detection of extracellular matrix components [], collagen crosslink [] and degradative enzymes [,] to explain the matrix disturbances, and detection of the expression of various cytokines to account for the deregulation of cellular activities [,]. Calcified tendinitis exhibited abnormal tendon calcification which is more common in rotator cuffs []. Recently, the findings of increased innervations [] and nociceptive substances [,] suggest that the chronic pain of tendinopathy may directly be resulted from the pathological changes. The findings of increased apoptosis [,] and acquisition of chondrogenic phenotypes [] in the injured tendons suggested a disturbance in cell differentiation. Increased proteoglycans with over-sulphation [] and expression of different versican variant [] may be related to abnormal chondrogenesis in the affected tendons. In contrast to early observations of a lack of inflammatory cells [], increased mast cell number was reported in human patellar tendinopathy []. Researchers are well aware of the limitation of the clinical samples, which may represent only the end-stage of the pathological processes with unknown duration and onset. Nevertheless, these observations have provided some direct clues to work out the pathogenesis of tendinopathy, and these histopathological characteristics are often used as endpoints in animal models of tendinopathy []. It should be noted that some of these pathological characteristics are sustained healing responses that failed to repair the initial injury, such as increased cell proliferation and elevated cytokines, which is also implicated in the normal healing process, as shown in the active remodeling sites in healthy tendons []. The histopathological features of tendinopathy we observed in animal models must be chronic and cannot be resolved spontaneously as compared to the normal course of tendon healing.

Genetic predisposition of tendinopathy

The possible genetic predisposition for Achilles tendinopathy has been investigated. It was found that variants within COL5A1 [], tenascin C [] and matrix metalloproteinase 3 (MMP3) gene [] was associated with increased risk of Achilles tendon injuries in general. Since these genes are related to homeostasis of extracellular matrix in tendons, it is suggested that the genetic variants modify the susceptibility of tendons to matrix disturbance observed in tendinopathy.

Evaluation of interventions to tendinopathy

The observed pathological changes of tendinopathy intuitively provided a lot of insights for the treatments. However, all current treatment methods may not significantly affect the natural history of the disease []. Surgical excision was reported to be used on animals over many years, in particular on horses []. Surgical excision of pathological tissues [,] and percutaneous multiple longitudinal incisions [,] were reported to be effective to relieve the symptoms similar to open excision of macroscopic pathologic tendon structures []. But ultrasonographic anomalies may still be evident in the healing tissues after surgical excision of pathological tissues; despite the painful symptoms were relieved []. Thus the current understanding of the relationship of structural changes and functional impairments is still inadequate to assure the degenerative features as specific “markers” for tendinopathy. Biophysical intervention such as extracorporeal shockwave therapy exhibited significant improvement especially for calcified tendinopathy [,]. It suggests that the pathological tissues might be responsive to mechanical stimulation. The observed effects of eccentric exercise for tendinopathy [,] also implied that a proper modulation of mechanical environment may exert positive effects on the diseased tendons, such as an increase in peritendinous collagen synthesis []. Other biophysical interventions included ultrasound therapy [], pulsed magnetic field therapy [,], low level laser therapy [], radiofrequency [] and acupuncture []. These studies claimed that modulation of inflammatory or neuronal components in the pathological tissues may exert beneficial effects. There are also reports on the use of nitric oxide [], sclerosing agents [,], MMP inhibitors [], bone marrow plasma injection [], autologous blood injection [,] or platelet-rich plasma [] for tendinopathy. Stem cell therapy was tried in horse models []. These studies may suggest the involvement of disturbances in cytokines, neovascularization, innervations or cell differentiation in the pathogenesis of tendinopathy.

Animal models of tendinopathy

The lack of a representative animal model is a major obstacle for tendinopathy research. Recent reviews discussed current animal models used for tendinopathy research [], including cytokine-induced tendon injuries [,,], collagenase-induced injury [,] and overuse induced injury [,]. Generally, histopathological characteristics derived from clinical samples are the main criteria for evaluation of tendinopathic changes. Ultrasonographic features were occasionally used in horse models [], and some studies reported pain-associated behavioral changes associated with the tendon injuries [,]. These animal models were established according to different hypotheses of pathogenesis, and aimed at reproducing the clinical signs of tendinopathy as far as possible. The use of cytokines to induce pathological changes implied the key roles of one or several cytokines in the development of the disease; while collagenase injection mimicked the pathological processes from the point when progressive matrix degradation was dominating. These chemically-induced tendinopathy models may reveal different starting points of the pathological process but the causes of increased cytokines or collagenases must be linked with clinically relevant etiological factors. Moreover, the acute induction of degenerative changes in these models cannot reflect the chronic development of the disease. On the other hand, animal models of overuse tendon injuries gained wide acceptance for the demonstration of the relationship between the mechanical overload and the development of histopathological changes [,,] and increase in pro-inflammatory mediators [,,]. Although overuse is sufficient to generate degenerative changes over a longer period of time, this form of injuries can be healed when the overuse training was ceased []; while in clinical cases of tendinopathy the symptoms were not improved by rest. Obviously, overuse tendon injury does not equate to tendinopathy. The failed healing response to the injuries caused by mechanical overload of tendons should also be considered in the establishment of animal model of tendinopathy. With respect to the variability in clinical manifestation of tendinopathy, most animal models may only mimic parts of the pathogenesis pathways, or they may only represent one of the possible pathways from the generation of injuries to development of tendinopathy features (Table (Table1).1). In summary, it appears that degenerative tendon injuries can be resulted from repetitive strain injuries that exceed the normal thresholds (overuse); while abnormal levels of cytokines and collagenases could be the effectors to mediate this kind of degenerative injuries.

Cell culture studies of effects of risk factors on tendinopathy

Cell culture studies of tendinopathy included the characterization of abnormal activities in the cells isolated from pathological tissues of tendinopathy [,,,], and the studies in normal cultured tendon cells in response to potential risk factors such as mechanical strain [] and xenobiotics []. In cell cultures of tendinopathy tissues, the abnormal cellular activities were persistent during sub-cultures, indicating relatively stable cell phenotypes that are significantly different from tendon fibroblasts derived from healthy tendons [,]. On the other hand, numerous studies showed that repetitive mechanical stimulation can affect production of pro-inflammatory mediators [,,,], metalloproteinases [,] and matrix syntheses [] in cultured tendon fibroblasts; while non-tenogenic differentiation of tendon derived stem cells can also be triggered by mechanical stretching []. Corticosteroids also induced fibrocartilage phenotype in tendon cells [], affected matrix synthesis [], cell viability [,] and apoptosis []. Fluoroquinolones may also activate metalloproteinases in tendon cells and hence collagenolytic injuries []. These observations implied that activation of collagenolysis and erroneous differentiation may weaken the mechanical properties of tendons []. Interestingly, non-steroidal anti-inflammatory drugs (NSAIDs) also modulate tendon cell proliferation [,], the expression of extracellular matrix components [] and degradative enzymes []. As NSAID is commonly used for sports-related injuries and symptoms, it is possible that anti-inflammatory treatment used for overuse injury may contribute to the development of tendinopathy [] which is normally diagnosed after NSAID treatment was failed.

Previous theories of pathogenesis of tendinopathy

Several theories of pathogenesis of tendinopathy have been proposed to explain the development of the histopathological features observed in the clinical samples of tendinopathy. Burry suggested that tendon lesions were not resolved properly and resulted in degenerative changes already in 1978 []. However, further elaboration of the idea of “improper resolution of tendon lesion” was not possible due to a lack of experimental evidences at that time. Leadbetter and Khan et al. have suggested that “tendinosis” are degenerative changes resulting from increased demand on tendons with inadequate repair and progressive cell death [,]. This model explained the generation of overuse injury, and the reasons for inadequate repair are attributed to adaptive response to tissue overload as elaborated by Kibler and Sorosky et al [,]. However, “inadequate repair” as quantitative decrease in healing cells cannot explain the findings of focal hypercellularity, active proliferation and metaplasia in tendinopathy samples. The “apoptosis theory” [] proposed by Murrell also neglect the fact of increased cellularity; but this hypothesis linked up oxidative stress, acquisition of cartilage phenotype and activation of metalloproteinase with the development of degenerative injuries by high dose of cyclic strain. Unfavorable mechanical stimulation as repetitive tensile strain [], stress-shielding [], contractile tension overloads [] or compression [] was proposed as noxious triggers on tendon cells to induce tendon inflammation or degenerative changes. These theories pointed out that the interactions between tendon cells and their mechanical environment were deterministic for the pathogenesis. On the other hand, Pufe et al. suggested that hypoxia and increased vascular in-growth into tendons may be the causes of tendon weakening and ruptures [], while Riley provided a neurogenic hypothesis to explain the adaptive responses to mechanical overload by nerve and mast cells unit [] and Fredberg et al. suggested neurogenic inflammation may be involved in the pathogenesis pathway []. These theories were formulated according to the findings of hypervascularity and increased innervations. In summary, the common motifs in these pathogenesis theories include unfavorable mechanical loading, adaptive cellular responses (including tendon, blood vessels and nerves) and the generation of histopathological features. In our opinion, it is possible to unify these ideas as “failed healing”, which may be the integral part of various pathological processes that divert various tendon injuries into its different manifestations of tendinopathy. (Table (Table11)

A unified theory of pathogenesis of tendinopathy

Based on the information of various lines of investigation of tendinopathy, we can summarize some major points which must be considered in the formulation of the pathogenesis model of tendinopathy:

1. The interactions of tendon injuries and unfavorable mechanical environment would be the starting point of the pathological process. Instead of coining the phrase “adaptive responses of tendon cells”, we think that the “adaptive healing responses to tendon injuries” would be a more comprehensive descriptor, which also includes vascular, neural and peri-tendinous reactions at different stages of healing.

2. The normal healing processes are diverted to an abnormal pathway, probably due to unfavorable mechanical environment, disturbances of local inflammatory responses, oxidative stress or pharmacological influences. Therefore, the healing capacity is not only inadequate but also incorrect and deviated from an ideal healing outcome.

3. The primary results of pathology are the progressive collagenolytic injuries co-existing with a failed healing response, thus both degenerative changes and active healing are observed in the pathological tissues.

4. These pathological tissues may aggravate the nociceptive responses by various pathways which are no longer responsive to conventional treatment such as inhibition of prostaglandin synthesis; otherwise the insidious mechanical deterioration without pain may render increased risk of ruptures.

Based on these points, we propose that the pathogenesis of tendinopathy can be perceived as a 3-stages process: injury, failed healing and clinical presentation. The first stage does not involve pathological changes and normal healing response could occur. The second stage is relatively insidious and discriminated from the third stage when clinical presentations are evident, such as ruptures or chronic pain, often resistant to conservative treatments.

Our theory of the pathogenesis of tendinopathy is summarized in Figure Figure11.

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Failed healing theory for the pathogenesis of tendinopathy.

Stage 1. Injury

In the first stage, initiation of tendinopathy may involve generation of collagenolytic injuries. Overuse can evoke the release of pro-inflammatory mediators [], which would result in stimulation of metalloproteinases and hence collagenolytic injuries [,]. Recent findings showed that the expression of MMP and tissue inhibitor of metalloproteinase (TIMP) in tendon cells were sensitive to mechanical overload or stress-deprivation [,]. MMP inhibitor suppressed development of mechanical weakness induced by stress-deprivation []. Chemicals such as fluoroquinolone can induce tendon cell death [], oxidative damages [] and collagenolysis []. A previous traumatic injury that has not been healed may also be susceptible to failed healing []. With the case reports of infectious tenosynovitis [], the involvement of pathogens to generate tendon injuries and inflammation could not be ruled out. Tendon pain and mechanical weakness is not significant at this stage and it is possible for the tendon injury to heal spontaneously.

Stage 2. Failed healing

In the failed healing stage, healing responses were activated but failed to repair the collagenolytic injuries. The exact causes for failed healing are still obscured. It is speculated that unfavorable mechanical environment, genetic pre-disposition, hormonal background and pharmacological exposures may affect the healing process. Since tendon healing includes many sequential processes such as inflammation, neovascularization, neural modulations [], recruitment of healing cells, proliferation, apoptosis [], matrix synthesis, tenogenic differentiation and matrix remodeling; disturbances occurred at different stages of healing may lead to different combinations of histopathological changes as what we observed in the clinical samples of tendinopathy (Table (Table1).1). Inflammatory responses are presumably elicited as the initial stage of tissue repair, but it may not be properly resolved under hostile mechanical environment or pharmacological intervention such as NSAIDs, resulting in elevated pro-inflammatory cytokines and a lack of ordinary inflammatory infiltration in the diseased tissues. Depending on the anatomical variations of the affected tendons, peritendinous reactions may be resulted as restrictive fibrosis, increased innervations and vascular in-growth from para-tenon structures may also take part in healing process []. The sustained activation of tendon progenitor cells with unfavorable micro-milieu for tendogenic differentiation may prone to erroneous differentiation into fibrochondrogenic [] or calcifying phenotypes [], which are normally confined to the regions of bone-tendon junctions. Tendon pain becomes significant and conservative treatments such as NSAIDs are prescribed to the patients, which may further modify the pathways of the failed healing.

Stage 3. Clinical presentation

In the third stage, symptomatic tendinopathy is diagnosed as longstanding, activity-related pain with characteristic medical images; while spontaneous ruptures are resulted from mechanical weakness under normal activities in cases of asymptomatic tendinopathy. The consequences of failed healing to collagenolytic injuries involve significant changes in extracellular matrix, which are then visible under ultrasound or MRI. In symptomatic cases, inflammatory pain may be involved and controlled during the injury and failed healing stages, but the pain mechanism may gradually shift to non-phlogistic ones such as agitation to peritendinous nerves by nociceptive substances or swelling, rendering the resistance to common anti-inflammatory treatments. Though mechanical weakness may be involved in asymptomatic cases [], lower activities due to pain may reduce risk of ruptures. In asymptomatic cases, the matrix disturbance resulted from failed healing may not activate nociceptive response. The insidious deterioration in mechanical properties of the affected tendons may lead to ruptures. Owing to different combinations of etiological factors, temporal and spatial variations on the failed healing, the clinical manifestations of tendinopathy may exhibit high variability.

Explicability of the theory

With this theory for the pathogenesis of tendinopathy, we can explain the process of the generation of the pathological features of tendinopathy we observed in the clinical samples. The theory is in accordance with most of the evidences derived from tendinopathy studies. For example, overuse is a major etiological factor but there are tendinopathy patients without obvious history of repetitive injuries. It is possible that non-overuse tendon injuries may also be exposed to risk factors for failed healing and entered to the third stage of tendinopathy. Overuse induces collagenolytic tendon injuries and it also imposes repetitive mechanical strain which may be unfavorable for normal healing. Stress-deprivation also induces MMP expression and whether over- or under-stimulation is still an active debate []. It is possible that tenocyte is responsive to both over- and under-stimulation, both tensile and compressive loading. Because the cellular responses of healing tendon cells change in different stages of tendon healing [], we speculate that the cell responsiveness to mechanical loading may not be constant during tendon healing and failed healing may be resulted from a mismatch of healing stages and the mechanical environment. Our theory can also explain why animal models of collagenase-induced injuries can reproduce the histopathological characteristics and functional impairment similar to tendinopathy; despite the generation of collagenolytic injuries in these models are completely different from the insidious onset of tendinopathy. By proposing a process of failed healing to translate tendon injuries into tendinopathy, other extrinsic and intrinsic factors would probably enter the play at this stage, such as genetic predisposition, age [], xenobiotics (NSAIDs and corticosteroids) and mechanical loading on the tendons. For example, differential tensile forces acting on patellar tendon [] may impose varying loading on tendon cells in different regions, it may explain why posterior proximal patellar tendon is pathological in patellar tendinopathy. Peritendinous structures may be disturbed to different extents in the healing response to tendon injuries, which may lead to different manifestations of “paratenonitis” or tendon adhesion. Investigations of how these factors affect tendon healing could help to further elucidate the mechanism of failed healing. The recent discovery of tendon-derived stem cells and characterization of pathological tissues of tendinopathy have provided evidences to support the ideas of erroneous cell differentiation that contribute to failed tendon healing. According to this theory of pathogenesis, we shall have a theoretical framework to develop a more representative animal model of tendinopathy for further study and verification. New ideas for treatments of tendinopathy may be inspired based on this theory, for example, a treatment which could override on the failed healing tissues and restart the healing process.

Missing links and limitations

As compared to previous theories of pathogenesis for tendinopathy which described a viscous cycle of inadequate repair and increased susceptibility of further injuries, this new theory attempts to describe the “vicious cycle” as an interaction between the vulnerability of the healing process to noxious mechanical and biochemical environments. Thus we can investigate the missing links as predicted in the theory, for example, the impact of mechanical stimulation on the cell differentiation of healing tendons cells, and the disturbances in cytokines triggered by re-injury on healing tendons. However, there are still some limitations in the current pathogenesis theory. Firstly, tendinopathies in different tendons exhibited specific patterns of affected regions and different forms of matrix disturbance, which may be presumably accounted by variations in local mechanical environment and vascular supplies; but it is difficult to explain for these variations at the present stage. Secondly, the interplay among innervations, increased nociception and tendon healing is unknown. It is still a black box for the mechanism of increased nociception by failed tendon healing. The factors which govern the development of chronic pain in tendinopathic tendons remain obscure. Finally, the interactions between healing tendons and the peritendinous tissues are seldom investigated and it is difficult to evaluate the potential involvement of peritendinous tissues in the development of tendinopathy.

Conclusions

In summary, we propose a unified theory for pathogenesis of tendinopathy which explain most of the available experimental data about tendinopathy. It is a just a start to probe into the nature of the pathology and we certainly wait for new findings and challenges to this theory until we finally find the truth.

 

WETENSCHAPPELIJKE PUBLICATIES OVERGENOMEN UIT PUBMED
feiten bestaan niet, alleen interpretaties. (Nietzsche)
wetenschappelijke publicaties over tennisarm -tenniselleboog etiologie

– Clin J Sport Med  2001 Oct;11(4):214-22
Corticosteroid injection in early treatment of lateral epicondylitis .

Newcomer KL, Laskowski ER, Idank DM, McLean TJ, Egan KS.
Department of Physical Medicine and Rehabilitation, and Section of Biostatistics, Mayo Clinic, Rochester, Minnesota 55905.

OBJECTIVE: To analyze whether a corticosteroid injection in combination with rehabilitation early in the course of lateral epicondylitis (LE) alters the outcome up to 6 months after injection compared with a control injection and rehabilitation.

DESIGN: Randomized, controlled, double-blind study. SETTING: Sports medicine center in a tertiary care center. PARTICIPANTS: Subjects with a diagnosis of LE whose symptoms had been present less than 4 weeks were included. Subjects were recruited by word of mouth and through advertising. The 39 subjects who were recruited were 18 to 65 years old. INTERVENTIONS: 19 subjects were randomized to receive rehabilitation and a sham injection, and 20 were randomized to receive rehabilitation and a corticosteroid injection. At 4 and 8 weeks, they were reevaluated and their treatment programs were modified, if indicated. MAIN OUTCOME MEASURES: Outcome measurements were performed at baseline, 4 weeks, 8 weeks, and 6 months, and included a functional pain questionnaire and a visual analogue pain scale. Painless grip strength on the affected side and maximal grip strength bilaterally were measured at baseline, 4 weeks, and 8 weeks. RESULTS: There were no significant differences in outcome between the two groups with the exception of an improvement in the visual analogue pain scale in the corticosteroid group from 8 weeks to 6 months. Outcome measurements in both groups improved significantly over time; more than 80% of subjects reported improvements from baseline to 6 months for all scales. CONCLUSION: A corticosteroid injection does not provide a clinically significant improvement in the outcome of LE, and rehabilitation should be the first line of treatment in patients with a short duration of symptoms.

-Publication Types: Clinical Trial Randomized Controlled Trial PMID: 11753057 [PubMed – indexed for MEDLINE]
What are the disadvantages and side effects of cortisone injections?

Disadvantages of cortisone injections are the necessity of piercing the skin with a needle as well as potential short and long term side effects. It should be emphasized that each of these side effects is possible, they usually do not occur.

Short term side effects are uncommon, but include shrinkage (atrophy) and lightening of the color (depigmentation) of the skin at the injection site, introduction of bacterial infection into the body, local bleeding from broken blood vessels in the skin or muscle, soreness at the injection site, and aggravation of inflammation in the area injected because of reactions to the corticosteroid medication (postinjection flare). Tendons can be weakened by corticosteroid injections in or near tendons. Tendon ruptures as a result have been reported.
In persons who have diabetes, cortisone injections can elevate the blood sugar. In patients with underlying infections, cortisone injections can suppress somewhat the body’s ability to fight the infection and possibly worsen the infection or may mask the infection by suppressing the symptoms and signs of inflammation. Generally, cortisone injections are used with caution in persons with diabetes and avoided in persons with active infections. Cortisone injections are used cautiously in persons with blood clotting disorders.
Long-term side effects of corticosteroid injections depend on the dose and frequency of the injections. With higher doses and frequent administration, potential side effects include thinning of the skin, easy bruising, weight gain, puffiness of the face, elevation of blood pressure, cataract formation, thinning of the bones (osteoporosis), and a rare but serious damage to the bones of the large joints (avascular necrosis).

– Scand J Med Sci Sports  2001 Dec;11(6):328-34
Non-operative treatment regime including eccentric training for lateral humeral epicondylalgia .
Svernlov B, Adolfsson L.
Department of Plastic Surgery, Hand Surgery and Burns, University Hospital,Linkoping, Sweden.
In a pilot study 38 patients with lateral humeral epicondylalgia were randomly allocated to two treatment groups. Group S (stretching) was treated with a contract-relax-stretching program while group E (eccentric exercise) underwent an eccentric exercise program. Both groups also received forearm bands and wrist support nightly. The programs were carried out daily at home during 12 weeks. Evaluation before and 3, 6 and 12 months after treatment, included subjective assessment of symptoms using visual analogue scales and grip strength measurements. Thirty-five patients were available for follow-up. Five patients, three in group S and two in group E, did not complete the programs due to increased pain while 30 (86%) reported complete recovery or improvement. Reduced pain and increased grip strength were seen in both treatment groups but 12 out of 17 patients (71%) in group E rated themselves as completely recovered as compared to 7 out of 18 (39%) in group S (P=0.09), and in group E the increase in grip strength after 6 months was statistically significantly larger than in group S. In a second study the eccentric training regime was used in a consecutive series of 129 patients with lateral epicondylalgia. The patients were divided into two groups with one group consisting of patients with less than one year duration of symptoms and the other comprised patients with a duration of symptoms for more than one year. The results of treatment were evaluated in the same way as in the pilot study, and also after 3.4 years using the scoring system by Verhaar et al. At the end of the treatment period statistically significant improvements were seen in all VAS recordings and in grip strength. After 3.4 years 38% had excellent, 28% good, 25% fair and 9% poor results according to the score. In the self-rated outcome 54% regarded themselves as completely recovered, 43% improved, 2% unchanged and 2% worse. No significant differences were seen between patients with a duration of symptoms for more than one year compared to patients with symptoms for less than one year. The eccentric training regime can considerably reduce symptoms in a majority of patients with lateral humeral epicondylalgia, regardless of duration, and is possibly superior to conventional stretching. Publication Types: Clinical Trial
Randomized Controlled Trial

PMID: 11782264 [PubMed – indexed for MEDLINE]
– Arch Orthop Trauma Surg  2001 Jun;121(6):329-32

Surgical treatment of resistant tennis elbow. A prospective, randomised study comparing decompression of the posterior interosseous nerve and lengthening of the tendon of the extensor carpi radialis brevis muscle.

Leppilahti J, Raatikainen T, Pienimaki T, Hanninen A, Jalovaara P.Department of Surgery, Oulu University Hospital, Finland.
We compared decompression of the posterior interosseous nerve (PIN) and lengthening of the distal tendon of the extensor carpi radialis brevis (ECRB)for treatment of tennis elbow in a randomised trial of 28 patients. Fourteen underwent decompression of PIN and 14, lengthening of ERCB. The groups did not differ significantly with regard to age, sex and work activities. The average duration of preoperative symptoms was 23 months. The PIN was exposed in the groove between the brachioradialis and brachialis muscles and decompressed at the arcade of Frohse by means of a 1-2 cm incision through the supinator muscle. The ECRB tendon was lengthened by Z-plasty at the dorsilateral aspect of the forearm. No postoperative complications occurred. The outcome after the primary operation was successful in 50% of the PIN group and in 43% of the ECRB group. Four of the 5 patients with a poor outcome were reoperated in the former group and 3 in the latter. The overall outcome after a mean follow-up of 31 months after the primary operation was successful in 60% of the cases.
Publication Types:Clinical Trial Randomized Controlled Trial

PMID: 11482465 [PubMed – indexed for MEDLINE]
– Z Orthop Ihre Grenzgeb  2000 Nov-Dec;138(6):492-5

Effectiveness of epicondylitis bandages from the biomechanical viewpoint
an experimental study]
[Article in German] Schauss S, Helwig U, Karpf M, Plitz W. Department fur Orthopadie und chirurgische Orthopadie, Landeskrankenhaus Villach, Osterreich. QUESTIONS: During extension of the elbow joint (test measurement) and extension of the wrist (control measurement), maximal bandage pressure is desired on the extensor group of the forearm, especially of the M. extensor carpl radialis brevis (ECRB). Do the various commercial epicondylitis bandages produce a mechanical effect on the extensor group of the forearm and how do the maximal pressures of these bandages behave in direct comparison? Are the pressures produced clinically relevant? METHODS: Eleven different epicondylitis bandage constructions were examined for their biomechanical effects. The exerted pressure was measured continously during the above-mentioned movements. A fist-closing strength of ca. 30 N was maintained for the necessary pre-stressing of the forearm muscles. RESULTS: Strap-type bandages were the only bandages to produce adequately high pressures. Bands applied at pressures which approach those of the straps led to obstruction in bloodflow. Stocking designs showed no effect in respect to our study. CONCLUSION: Bandages which apply pressure to relieve the tendon insertion of the extensor muscles must, from a technical standpoint, be of a strap construction in order to build up adequate pressures to be effective.
PMID: 11199412 [PubMed – indexed for MEDLINE]

– Acta Orthop Scand  1997 Jun;68(3):249-54

Sarcomere length in wrist extensor muscles. Changes may provide insights into the etiology of chronic lateral epicondylitis.

Lieber RL, Ljung BO, Friden J. Department of Orthopedics, University of California, San Diego, USA.
Since the etiology of tennis elbow (lateral epicondylitis) is poorly understood, we studied the anatomical changes in the extensor carpl radialis brevis (ECRB) muscle during elbow joint rotation. Specifically, we measured ECRB sarcomere length, using an intraoperative laser diffraction procedure that measures muscle sarcomere length with an accuracy of +/- 0.05 micron. We found an unexpected biphasic response in ECRB sarcomere length as the elbow was rotated from full extension to full flexion. The initial sarcomere length of 3.49 microns, with the elbow extended, was gradually changed to 3.68 microns, 3.34 microns, 3.81 microns, and 3.45 microns with progressive elbow flexion. Based on the very nonlinear mechanical properties of skeletal muscle, this “double lengthening” of the ECRB during progressive flexion would impose intense eccentric contractions on the muscle itself. Given that eccentric contractions cause muscle injury and subsequent inflammation, these findings may provide insights into the etiology of lateral epicondylitis.
PMID: 9246987 [PubMed – indexed for MEDLINE]

-J Orthop Sports Phys Ther  1996 Apr;23(4):251-7

Radial epicondylalgia (tennis elbow): measurement of range of motion of the wrist and the elbow.

Solveborn SA, Olerud C. Department of Orthopaedics, Uppsala University Hospital, Sweden. The aim of the present investigation was to determine the range of motion (ROM)features of the elbow and wrist joints in patients with radial epicondylalgia (tennis elbow), since there have been contradictory statements in previous reports and apparently no accurate study has been published to establish these typical ROM values. The precision of the measuring technique and the active and passive ROMs of these joints were first evaluated in an intratester reliability study in 16 healthy individuals, 12 men and four women with a mean age of 46 years (range = 26-67). The clinical study consisted of 123 patients with unilateral symptoms, 75 men and 48 women with a mean age of 43 years (19-63) and a mean symptom duration of 11 months (0.5-72). All measurements were performed using a simple plastic goniometer. The precision of the measuring procedure, expressed as the standard deviation of the random error of the mean, was 1-6 degrees depending on the actual ROM measured. In patients with unilateral radial epicondylalgia, almost all measured ROMs of the elbow and wrist were found to be limited in the affected arm. This could give a rationale to use stretching in the treatment of radial epicondylalgia. 
PMID: 8775370 [PubMed – indexed for MEDLINE]

-Z Orthop Ihre Grenzgeb  1986 May-Jun;124(3):323-6
A diagnostic sign in so-called epicondylitis humeri radialis [Article in German] Coenen W .

With a simple test – the “finger-snapping-test” – it is possible to narrow down the etiology of lateral epicondylalgia of the humerus. On the basis of a groupof 196 patients it is shown that a positive result of this test is characteristic for an enthesopathy of the extensor carpi radialis brevis muscle, whose insertion is at the radial epicondyle. If the test is negative it must be assumed that the pain is caused by spondylogenic, arthrogenic, or neurogenic phenomena. The importance of the test for the therapeutic approach and with regard to the indication for operation after Hohmann ist pointed out. 
PMID: 3751247 [PubMed – indexed for MEDLINE]

-Clin Orthop  2002 May;(398):239-44

Arterial vascularization of the proximal extensor carpi radialis brevis tendon

. Schneeberger AG, Masquelet AC. Department of Orthopaedic Surgery, Balgrist, University of Zurich, Zurich, Switzerland; and the Department of Orthopaedic Surgery, University of Paris, Hopital Avicenne, Bobigny Cedex, France.
The macroscopic arterial vascularization of the extensor carpi radialis brevis tendon was investigated in 12 elbows from cadavers to provide fundamental anatomic information of this tendon which has been associated with lateral epicondylitis. The arterial blood supply of the extensor carpi radialis brevis tendon was highly consistent. The radial recurrent artery vascularized the entire proximal tendon through direct branches to the medial and lateral border of the tendon forming a network of small vessels on the surface of the tendon. Important contributions were provided by the posterior branch of the radial collateral artery, and minor contributions were provided by the interosseous recurrent artery. The undersurface of the tendon seemed almost avascular. This observation suggests that potential hypovascular zones might be located at theundersurface of the tendon causing degeneration and partial tear of the tendon, and that this might be an etiologic factor in the pathogenesis of lateral epicondylitis. Additional microvascular studies are necessary to investigate this hypothesis.  PMID: 11964656 [PubMed – in process]

-Eur J Histochem  2002;46(1):3-12
Morpho-functional changes in human tendon tissue.
Galliani I, Burattini S, Mariani AR, Riccio M, Cassiani G, Falcieri E.
Department of Human Anatomy, University of Bologna, Italy.
galliani@biocfarm.unibo.it

Insertion tissue biopsies of right arm common extensor tendons from 11 patients with chronic lateral epicondylitis were processed for light and electronmicroscopy. The subjects were aged between 38 and 54 years (only one was 25).The specimens showed a variety of structural changes such as biochemical and spatial alteration of collagen, hyaline degeneration, loss of tenocytes,fibrocartilage metaplasia, calcifying processes, neovascularization and vessel wall modifications. Tissue alterations were evident in limited zones of the tendon fibrocartilage in which the surgical resection was generally visible. The areas where the degenerative processes were localized, were restricted and inspatial contiguity with morphologically normal ones. The observed cases presented histological and electron microscopic findings that characterize lateral epicondylitis as a degenerative phenomenon involving all tendon components.
PMID: 12044045 [PubMed – in process]

Effect of elbow position on grip strength in the evaluation of lateral epicondylitis.
Dorf ER, Chhabra AB, Golish SR, McGinty JL, Pannunzio ME.
University of Virginia Hand Center, Charlottesville, VA, and Reconstructive Hand Surgeons of Indiana, Carmel, IN, USA.
PURPOSE: This study evaluated the maximum grip strength in a position of elbow extension versus flexion as a diagnostic tool in the assessment of a patient with suspected lateral epicondylitis (LE). METHODS: From our database we identified 81 patients with grip strength measurements and the diagnosis of LE. From these patient records we collected grip strength measurements with the elbow in full extension and with the elbow in 90 degrees of flexion for the affected and the healthy extremity. We then compared 2 values: the pretreatment grip strength in flexion and extension for the affected extremity and the pretreatment grip strengths of the nonaffected extremity compared with the affected extremity. Grip strengths were compared with paired and unpaired 2-tailed t tests. RESULTS: Grip strength was no different in flexion and extension for the healthy extremity and 29% stronger in flexion than in extension for the affected extremity. The affected arm averaged 50% of the strength of the healthy arm in extension and 69% of the strength of the healthy arm in flexion. These differences were statistically significant. An 8% difference in grip strength between flexion and extension was found to be 83% accurate in distinguishing the affected from the unaffected extremities. CONCLUSIONS: The measurement of extension grip strength is a useful objective tool to aid in the diagnosis of LE. In patients with LE, the grip strength decreases as one moves from a position of flexion to a position of extension.
PMID: 17606071 [PubMed – indexed for MEDLINE]

Anatomic factors related to the cause of tennis elbow.
Bunata RE, Brown DS, Capelo R.
4054 Hildring Drive West, Fort Worth, TX 76109. rbunata@hsc.unt.edu.
BACKGROUND: The pathogenesis of lateral epicondylitis remains unclear. Our purpose was to study the anatomy of the lateral aspect of the elbow under static and dynamic conditions in order to identify bone-to-tendon and tendon-to-tendon contact or rubbing that might cause abrasion of the tissues. METHODS: Eighty-five cadaveric elbows were examined to determine details related to the bone structure and musculotendinous origins. We identified the relative positions of the musculotendinous units and the underlying bone when the elbow was in different degrees of flexion. We also recorded the contact between the extensor carpi radialis brevis and the lateral edge of the capitellum as elbow motion occurred, and we sought to identify the areas of the capitellum and extensor carpi radialis brevis where contact occurs. RESULTS: The average site of origin of the extensor carpi radialis brevis on the humerus lay slightly medial and superior to the outer edge of the capitellum. As the elbow was extended, the undersurface of the extensor carpi radialis brevis rubbed against the lateral edge of the capitellum while the extensor carpi radialis longus compressed the brevis against the underlying bone. CONCLUSIONS: The extensor carpi radialis brevis tendon has a unique anatomic location that makes its undersurface vulnerable to contact and abrasion against the lateral edge of the capitellum during elbow motion. CLINICAL RELEVANCE: This information may help us to understand the pathomechanics of lateral epicondylitis and provide a better rationale for operative and nonoperative treatment.
PMID: 17768192 [PubMed – in process]

-Zeisig E; Ohberg L; Alfredson H

Tennis elbow, extensor carpi radialis brevis (ECRB) tendinosis, is a condition with unknown etiology and pathogenesis, known to be difficult to treat. The pain mechanisms have not been fully clarified, but involvement of a neurogenic inflammation mediated via the neuropeptide Substance-P (SP), has been suggested. In this investigation, grey-scale ultrasonography (US) and colour Doppler (CD) was used to examine the common extensor origin in 17 patients with the diagnose Tennis elbow in altogether 22 elbows, and in 11 controls with 22 pain-free elbows. In 21/22 elbows with chronic pain from the extensor origin, but only in 2/22 pain-free elbows, vascularity was demonstrated in the extensor origin. After US and CD-guided injection of a local anaesthetic, targeting the area with vessels, the patients were pain-free during extensor-loading activity.The area with vascularity found in the extensor origin seems to be related to pain. Most likely, the findings correspond with the vasculo-neural in growth that has been demonstrated in the chronic painful Achilles tendon, and possibly have implications for treatment.

-An isokinetic eccentric programme for the management of chronic lateral epicondylar tendinopathy Jean-Louis Croisier, Marguerite Foidart-Dessalle, France Tinant,

Background: Lateral epicondylitis represents a frequent overuse injury. In spite of many conservative treatment procedures, prolonged symptoms and relapse are frequently observed.

Objective: To compare the outcome of patients performing an isokinetic eccentric training with that of age-, gender-, activity-matched patients receiving a non-strengthening classical rehabilitation.

Methods: Ninety-two patients with unilateral chronic lateral epicondylar tendinopathy (mean duration of symptoms 8±3 months) were assigned either to a control group (n = 46) or to an eccentrically trained group (n = 46). The control group underwent a passive standardised rehabilitation programme that excluded strengthening exercises. In addition to this programme, the trained group also performed eccentric exercises based on the repetitive lengthening of the active musculo-tendinous unit. The latter exercises started with submaximal contraction intensity and slow speed movement. Modalities were progressively intensified (increase in intensity contraction and speed movement) over a long priod of treatment. Programme effectiveness was assessed through pain score evaluation, a disability questionnaire, muscle strength measurement and ultrasonographic examination.

Results: Compared to the non-strengthening control group, the following observations were made in the eccentrically trained group: (1) a significantly more marked reduction of pain intensity, mainly after one month of treatment; (2) an absence of strength deficit on the involved side through bilateral comparison for the forearm supinator and wrist extensor muscles; (3) an improvement of the tendon image as demonstrated by decreasing thickness and a recovered homogenous tendon structure; and (4) a more marked improvement in disability status during occupational, spare time and sports activities.

Conclusion: These results highlight the relevance of implementing isokinetic adapted eccentric training in the management of chronic lateral epicondylar tendinopathy.
COMPARISON OF EFFECTS OF CYRIAX PHYSIOTHERAPY, A SUPERVISED EXERCISE PROGRAMME AND POLARIZED POLYCHROMATIC NON-COHERENT LIGHT (BIOPTRON LIGHT) FOR THE TREATMENT OF LATERAL EPICONDYLITIS

-Stasinopoulos D, Stasinopoulos I.Clin Rehabil 2006;20:12–23
Background: There are many possible therapeutic interventions for lateral epicondylopathy (tennis elbow), including physiotherapy, exercise rehabilitation and, recently, polarised polychromatic non-coherent (Bioptron) light.
Research question/s: What is the effectiveness of Cyriax physiotherapy, a supervised exercise and polarised polychromatic non-coherent light (Bioptron light) in the treatment of lateral epicondylitis?
Methodology:Subjects: 75 patients with clinically diagnosed lateral “epicondylitis.
Experimental procedure: Subjects were sequentially allocated to 3 treatment (3/week) groups for 4 weeks: Cyriax physiotherapy (CP = 25), supervised exercise (EX = 25) and polarised polychromatic non-coherent light (Bioptron light) (BIOP = 25). Pain, function and grip strength were assessed before and after 4, 8, 16 and 28 weeks.
Measures of outcome: Pain (visual analogue scale; VAS), function (VAS), pain-free grip strength.
Main finding/s:: Improvement of function was also greatest in the EX group compared with the other groups at any of the follow-up time points (p<0.05).
Conclusion/s: Compared with Cyriax physiotherapy or polarised polychromatic non-coherent light (Bioptron light), a supervised exercise programme was superior in pain reduction and improved function in the management of patients with lateral epicondylitis.

-J Hand Surg Br. 2002 Oct;27(5):405-9.
The role of the extensor digitorum communis muscle in lateral epicondylitis.
Fairbank SM,
A common finding in tennis elbow is pain in the region of the lateral epicondyle during resisted extension of the middle finger (Maudsley’s test). We hypothesized that the pain is due to disease in the extensor digitorum communis muscle, rather than to compression of the radial nerve or disease within extensor carpi radialis brevis. Thirteen human forearm specimens were examined. It was found that the extensor digitorum communis was separable into four parts. The part to the middle finger originated from the lateral epicondyle, but the muscle slips to the other fingers originated more distally. Pain ratings were measured in ten patients diagnosed with lateral epicondylitis during isometric finger and wrist extension tests. The results confirmed the high prevalence of a positive Maudsley’s test in lateral epicondylitis, and also that the patients with tenderness at the site of origin of the extensor digitorum communis slip to the middle finger had the greatest pain during middle finger extension.These anatomical and clinical findings clarify the anatomy of extensor digitorum communis, and suggest that this muscle forms the basis for the Maudsley’s test. The muscle may play a greater role in tennis elbow than previously appreciated.PMID:12367535 [PubMed – indexed for MEDLINE]

Comparison of scapular position and upper extremity muscle strength in patients with and without lateral epicondylalgia: a case-control study.

Ucurum SG1, Karabay D2, Ozturk BB3, Kaya DO2.

Abstract

BACKGROUND:

The symptoms of lateral epicondylalgia (LE) can be persistent, and recurrence is frequent. Recurrence can be related to proximal segment impairment of the kinetic chain. Knowledge of any relation in the kinetic chain in LE may help treatment. We aimed to investigate scapular position and upper extremity muscle strength in patients with LE and to compare them with controls.
METHODS: The study enrolled 51 patients with LE and 51 age-matched controls. We assessed scapular position asymmetry using the lateralscapular slide test and measured the strength of the upper trapezius (UT), middle trapezius (MT), lower trapezius, and serratus anterior muscles in addition to shoulder abduction, external rotation, and internal rotation and grip strength.
RESULTS: The percentage of participants with scapular asymmetry was greater in the patients than in the controls (P = .005). The involved side regarding shoulder external rotation among the patients was significantly weaker than in the controls (P = .016, P = .009). The involved side of the LE patients was significantly weaker than the uninvolved side in terms of shoulder abduction, external rotation, and internal rotation (P = .013, P = .048, P = .013). The UT/MT ratio on the nondominant side of the controls was significantly greater than that on the involved side of the LE patients (P = .016).
CONCLUSION: Upper extremity muscle strength, grip strength, UT/MT ratio, and scapular position are affected in patients with LE. In addition to the elbow, focusing on the upper segments is essential in the management of LE.

 

Efficacy of extracorporeal shockwave therapy in patients with lateral epicondylitis: A randomized, placebo-controlled, double-blind clinical trial.

Guler NS1, Sargin S2, Sahin N1.

OBJECTIVE: Lateral epicondylitis is a common elbow problem. Although extracorporeal shockwave therapy (ESWT) is widely used in the treatment of lateral epicondylitis, its efficacy is still controversial. Moreover, the number of prospective, randomized, controlled studies in the literature is not sufficient. Here, we intend to investigate the efficacy of ESWT. ,
METHODS: The study was randomized, placebo-controlled, double-blind, and prospectively planned. Forty patients who met the inclusion criteria were divided into two groups, real ESWT (Group 1, n=20) and placebo ESWT (Group 2, n=20), in a 1: 1 randomized closed envelope manner. Patients were evaluated for Patient-Rated Tennis Elbow Evaluation-Turkish Version (PRTEE-T), visual analog scale (VAS) pain scores, and grip and pinching strengths. The evaluation were performed thrice before, at the end of treatment and 1 month after treatment. Both groups were treated with wrist splinting, ice treatment, and rest.
RESULTS: There was no statistical difference between sex and dominant hand in both groups. There was no significant difference in the grasp and pinching strength between the measurements of the groups themselves (p>0.05). When examined in terms of VAS scores, only significant changes were found in the actual ESWT group (p<0.05). According to the PRTEE-T scores, both groups showed significant changes (p<0.05). No significant difference was found between post-treatment and control measures in the grip and pinching power between groups, VAS and PRTEE-T scores before treatment (p>0.05).
CONCLUSION: Although pain and functional improvement were more prominent in our patients treated with ESWT than placebo, no statistically significant results were found.

 

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